Perinatal asphyxia is an important cause of brain injury. It may
lead to hypoxic-ischaemic encephalopathy (HIE) which occurs in one to
six of every 1000 full term births. The risk of death or severe handicap is
0.5-2.0 out of 1000. Following intrapartum asphyxia cerebral hypoperfusion
in combination with hypoxia produces characteristic neuropathological
changes and related clinical signs. After the primary insult
there is a thirty minutes period of reperfusion characterized by the partial
recovery of cell and metabolic processes. This is followed by a latent
phase which may last up to six hours. In this phase oxidative metabolism
(near) normalizes (shown by MRspectroscopy) but EEG activity is depressed
and the blood flow is likely to be reduced. Secondary energy failure
and secondary hyperperfusion (‘luxury perfusion’) may occur in the
neonatal brain within 6-15 hours after an acute ischaemic insult, marked
by the acute onset of seizures (peaking at about 12 hours post insult).
Excitotoxins accumulate in the cell and cell death may take 72 hours to
completion. The infant’s gestational age and thus the maturational
stage of the brain, as well as type, severity and duration of the insult are
determinants of the brain injury. During the insult there is redistribution
of blood flow to the brain, heart and adrenals. Our current understanding
of perinatal asphyxia is based on animal experiments. Different and
mixed etiologies lead to a range of post asphyxial patterns, usually subdivided
into different patterns; acute, chronic or a combination of these
two. With chronic, possibly repetitive insults, lesions are predominantly
seen in (sub)cortical structures. This has been named watershed injury
for its classical distribution along the borderzones between the major
pial arteries, sparing thalamus and basal ganglia. From the literature it
appears that watershed injury is observed most frequently in context
of term birth asphyxia. In acute and (near) total asphyxia the damage is
mostly to the thalami, basal ganglia, hippocampus, cerebellum, brain
stem and specific areas of the neocortex like the rolandic, calcarine and
insular cortex.http://repub.eur.nl/res/pub/19509/100422_Swarte%2C%20Renate%20Maria%20Cornelia.pdf
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